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PubMed1991

Alterations of GABA-A and dopamine D-2 brain receptors in dogs with portal-systemic encephalopathy.

The binding characteristics of gamma-aminobutyric acid-A (GABA-A) receptors and the kinetic characteristics of the target enzyme of GABA synthesis in nerve terminals, glutamic acid decarboxylase (GAD), were studied in a dog model of portal-systemic encephalopathy obtained by porta-caval shunt performed in dimethylnitrosamine pretreated animals. Furthermore the properties of dopamine receptors and the levels of catecholamines of encephalopathic dogs were investigated. The mild stage of encephalopathy was characterized by an up-regulation of the inhibitory GABA-A receptors probably related to a decrese of GABA in nerve terminals since GAD was decreased and by a slight decrease of catecholamines and by an increased synthesis of octopamine associated with a decreased affinity of dopamine receptors. In the severe stage there was a selection of high affinity GABA-A receptors with an increased number of benzodiazepine recognition sites which were supersensitive to GABA stimulation, a decreased number of Dopamine D-2 receptors and a marked reduction of catecholamines. These data seem to suggest that the neurological disturbances of experimental portal-systemic encephalopathy might be the result of an imbalance between inhibitory and excitatory systems leading to a prevalence of the first one.

Animals↗
PubMed1999

Manganese deposition in basal ganglia structures results from both portal-systemic shunting and liver dysfunction.

BACKGROUND & AIMS: Manganese (Mn) deposition could be responsible for the T(1)-weighted magnetic resonance signal hyperintensities observed in cirrhotic patients. These experiments were designed to assess the regional specificity of the Mn increases as well as their relationship to portal-systemic shunting or hepatobiliary dysfunction. METHODS: Mn concentrations were measured in (1) brain samples from basal ganglia structures (pallidum, putamen, caudate nucleus) and cerebral cortical structures (frontal, occipital cortex) obtained at autopsy from 12 cirrhotic patients who died in hepatic coma and from 12 matched controls; and from (2) brain samples (caudate/putamen, globus pallidus, frontal cortex) from groups (n = 8) of rats either with end-to-side portacaval anastomosis, with biliary cirrhosis, or with fulminant hepatic failure as well as from sham-operated and normal rats. RESULTS: Mn content was significantly increased in frontal cortex (by 38%), occipital cortex (by 55%), pallidum (by 186%), putamen (by 66%), and caudate (by 54%) of cirrhotic patients compared with controls. Brain Mn content did not correlate with patient age, etiology of cirrhosis, or history of chronic hepatic encephalopathy. In cirrhotic and portacaval-shunted rats, Mn content was increased in pallidum (by 27% and 57%, respectively) and in caudate/putamen (by 57% and 67%, respectively) compared with control groups. Mn concentration in pallidum was significantly higher in portacaval-shunted rats than in cirrhotic rats. No significant changes in brain Mn concentrations were observed in rats with acute liver failure. CONCLUSIONS: These findings suggest that brain Mn deposition results both from portal-systemic shunting and from liver dysfunction.

Animals↗
PubMed2000

The astrocytic ("peripheral-type") benzodiazepine receptor: role in the pathogenesis of portal-systemic encephalopathy.

An increasing body of evidence supports the notion that activation of astrocytic (peripheral-type) benzodiazepine receptors contributes to the pathogenesis of the central nervous system symptoms which are characteristic of portal-systemic encephalopathy (PSE). Binding site densities for the PTBR ligand [3H-PK11195] are increased in autopsied brain tissue from PSE patients as well as in the brains of animals with experimental chronic liver failure. In the case of the animal studies, increased PTBR sites resulted from increased PTBR gene expression. Exposure of cultured astrocytes to ammonia or manganese (two neurotoxic agents which under normal circumstances are removed by the hepatobiliary system and which are found to accumulate in brain in PSE) results in increased densities of [3H-PK11195] binding sites. Activation of PTBR is known to result in increased cholesterol uptake and increased synthesis in brain of neurosteroids some of which have potent positive allosteric modulator properties on the GABA-A receptor system. Accumulation of such substances in the brain in chronic liver failure could explain the neural inhibition characteristics of PSE.

Ammonia↗
PubMed1998

The basal ganglia and portal-systemic encephalopathy.

Despite decades of research, the pathogenesis of portal-systemic encephalopathy (PSE) remains puzzling. Current hypotheses on the pathophysiology of PSE usually deal with metabolic toxins like ammonia or disturbances in neurotransmitter systems, especially glutamatergic or GABA-ergic neurotransmission. With respect to clinical, neuropathological, MRI and PET findings this review advances the hypothesis that the known alterations of neurotransmission and astrocytic function in PSE might impair basal ganglia function in cirrhotics. The symptoms of PSE - whether cognitive, emotional or motor - are proposed to be a consequence of basal ganglia dysfunction.

Basal Ganglia↗
PubMed1995

Selective alterations of extracellular brain amino acids in relation to function in experimental portal-systemic encephalopathy: results of an in vivo microdialysis study.

Portal-systemic encephalopathy (PSE) is characterized by neuropsychiatric symptoms progressing through stupor and coma. Previous studies in human autopsy tissue and in experimental animal models of PSE suggest that alterations in levels of brain amino acids may play a role in the pathogenesis of PSE. To assess this possibility, levels of amino acids were measured using in vivo cerebral microdialysis in frontal cortex of portacaval-shunted rats administered ammonium acetate (3.85 mmol/kg, i.p.) to precipitate severe PSE. Sham-operated rats served as controls. Portacaval shunting resulted in significant increases of levels of extracellular glutamine (threefold, p < 0.001), alanine (38%, p < 0.01), aspartate (44%, p < 0.05), phenylalanine (170%, p < 0.001), tyrosine (140%, p < 0.001), tryptophan (63%, p < 0.001), leucine (75%, p < 0.001), and serine (60%, p < 0.001). Administration of ammonium acetate to sham-operated animals led to a significant increase in extracellular glutamine and taurine content, but this response was absent in shunted rats. The lack of taurine release into extracellular fluid following ammonium acetate administration in portacaval-shunted rats could relate to the phenomenon of brain edema in these animals. Ammonium acetate administration resulted in significant increases in the extracellular concentrations of phenylalanine and tyrosine in both sham-operated and portacaval-shunted rats. Severe PSE was not accompanied by significant increases in extracellular fluid concentrations of glutamate, aspartate, GABA, tryptophan, leucine, or serine, suggesting that increased spontaneous release of these amino acids in cerebral cortex is not implicated in the pathogenesis of hepatic coma.

Acetates↗
PubMed1994

Transjugular intrahepatic portal-systemic shunts (TIPS)--initial experience and clinical outcome.

BACKGROUND: The clinical role of the transjugular intrahepatic portal-systemic shunt (TIPS) has not been fully defined. AIMS: To determine the technical results of TIPS and the clinical outcome of patients undergoing the procedure. METHODS: Retrospective audit of the results of the first 31 procedures performed in Melbourne. RESULTS: Thirty procedures were performed for variceal haemorrhage, one procedure was for ascites. The aetiology of the liver disease was cirrhosis due to alcohol in 20, cryptogenic in five, chronic viral infection in four, and autoimmune chronic active hepatitis in one. Nodular regenerative hyperplasia was present in one patient. Seventy-seven per cent of procedures were considered successful based on the angiographic demonstration of shunt patency at the end of the procedure. The in-hospital mortality in all patients undergoing TIPS was 45% and was 42% in patients undergoing technically successful TIPS. Only age could be identified as predictive of death in hospital. In patients leaving hospital, we found a rebleeding rate of 57% with one patient dying of bleeding, one requiring balloon tamponade and two requiring variceal sclerotherapy. Hepatic trauma was documented in six cases, shunt thrombosis in four cases, stent displacement in two cases and severe hepatic encephalopathy in one case. CONCLUSIONS: TIPS has the potential to decompress the portal venous system, but the procedure is technically complex and should be performed in the knowledge that mortality and morbidity can be relatively high, particularly in patients whose condition is poor.

Adult↗
PubMed1976

Effect of portal-systemic anastomosis on renal haemodynamics in cirrhosis.

In 12 patients with portal hypertension and repeated bleedings from oesophageal varices the central haemodynamics, portal pressure, and mean renal blood flow (RBF) were investigated immediately before and two to seven months after portal-systemic shunt. Cardiac output increased significantly, whereas arterial pressure was unchanged after operation. RBF, which was initially less than in controls, did not change. As portal pressure decreased significantly, a direct portal-renal, neural, or humoral reflex mechanism does not explain the subnormal RBF in cirrhosis. As plasma volume was large and unchanged after operation a "diminished circulating plasma volume" is an unlikely explanation. Therefore, on the basis of the present observations, previously postulated causes of renal hypoperfusion in cirrhosis need revision.

Adult↗
PubMed1982

Treatment of chronic portal--systemic encephalopathy with vegetable and animal protein diets. A controlled crossover study.

A controlled crossover clinical comparison of 40-g/day and 80-g/day vegetable protein diets vs a 40-g/day meat protein diet plus neomycin-milk of magnesia (as control therapy) was performed on 10 cirrhotic patients with mild chronic portal-systemic encephalopathy. The 40-g vegetable protein diet had a high fiber volume and contained low methionine and low aromatic amino acids. The 80-g vegetable protein diet was rich in branched-chain amino acids and fiber, with a similar content of sulfur-containing amino acids as compared to the 40-g meat protein diet. Serial semiquantitative assessments were done, including mental state, asterixis, number connection tests, electroencephalograms and blood ammonia levels. No patient developed deep coma while ingesting either vegetable protein diet or neomycin-milk of magnesia plus 40-g meat protein diet. A significant improvement in the number connection test times was observed during the 40-g vegetable protein diet (P less than 0.05) and during the 80-g vegetable protein diet (P less than 0.05) as compared to their previous 40-g meat protein--neomycin periods. In addition, during the period of 80-g vegetable protein diet, the patients showed a significant improvement in their electroencephalograms (P less than 0.05). The frequency of bowel movements significantly increased (P less than 0.05) during the 80-g vegetable protein diet period. During the 40-g vegetable protein diet, two cirrhotic--diabetic patients experienced hypoglycemia. Three patients complained of the voluminous 80-g vegetable protein diet. Patients with mild portal--systemic encephalopathy may be adequately controlled with vegetable protein diets as a single therapy.

Adult↗
PubMed1992

[A case of portal-systemic encephalopathy presenting characteristic MR images in globus pallidus, hypothalamus, corpus callosum, pontine base, and middle cerebellar peduncle].

A 53-year-old woman developed symptoms of slow speech, mild dementia, increased deep tendon reflex, ataxic gait, flapping tremor, and dystonic posture during two years. She had liver cirrhosis and hyperammonemia, which suggested a diagnosis of portal-systemic encephalopathy. MR T1-weighted images showed increased signal intensity in globus pallidus, internal capsule, substantia innominata, and a part of hypothalamus. T2-weighted images revealed abnormal findings as follows: high intense area in middle cerebellar peduncle, and low signal intensity of corpus callosum and pontine base. This is the first report about MRI abnormalities in substantia innominata, corpus callosum, and pontine base in a patient with portal-systemic encephalopathy.

Brain↗
PubMed1984

Dietary protein supplementation from vegetable sources in the management of chronic portal systemic encephalopathy.

In a controlled cross-over trial, we have compared a conventional 40-g protein diet (30 g animal and 10 g vegetable, diet A) with an 80-g vegetable-protein-supplemented diet (30 g animal and 50 g vegetable, diet B) in the treatment of six patients with chronic stable portal systemic encephalopathy, requiring dietary and lactulose therapy. Each diet was given, in random order, for 5 days in hospital. EEG, clinical indices of encephalopathy, and the plasma amino acid profile were assessed at the end of each treatment period. The increase in vegetable protein intake was associated with minor improvement in EEG and clinical performance in two patients, and no change in the others. Fasting plasma phenylalanine and tyrosine were higher on diet B [phenylalanine 108.6 +/- 9.3 (SEM) mumol/L versus 99.6 +/- 8.37, p less than 0.05 (paired t test); tyrosine 153 +/- 15.2 mumol/L versus 140 +/- 14, p less than 0.05). The plasma branched-chain amino acid levels did not change, and the branched chain/aromatic amino acid ratio (BCAA/AAA) was lower on diet B (p less than 0.02). Fecal weights were not significantly altered. These results indicate that patients with chronic portal systemic encephalopathy are tolerant of protein supplementation from vegetable sources. A minor improvement in parameters of encephalopathy was seen in some individuals, despite a lowering of BCAA/AAA which some investigators have thought important in the pathogenesis of encephalopathy.

Adult↗
PubMedDate not supplied

Schistosoma mansoni: acquired resistance in mice by implantation of young irradiated worms into the portal system.

In two distinct experiments, immature S. mansoni worms (LE strain, Belo Horizonte, Brazil), aged 20 days, obtained from the portal system of white outbred mice, were irradiated with 14 and 4 Krad, respectively. Afterwards, the worms were directly inoculated into the portal vein of normal mice. Inoculation was performed with 20 irradiated worms per animal. Fifty days after inoculation, the mice that received 4 and 14 Krad-irradiated worms and their respective controls were infected with S. mansoni cercariae (LE strain), by transcutaneous route. Twenty days after this challenge infection, the animals were sacrificed and perfused for mature irradiated (90-day-old) and immature (20-day-old) worm counts. Analysis of the results showed that statistically significant protection against cercariae occurred in both groups with irradiated worms.

Animals↗
PubMed1978

[Surgical aspects of thrombosis in the portal system (author's transl)].

The Authors present and discuss clinical and therapeutic aspects of several cases of chronic portal thrombosis, troncular and radicular, either isolated or variously associated. Splenoportography and selective arteriography do not always provide a clear-cut picture of the vascular situation, particularly in the presence of mural thrombi. Surgery may be needed as an emergency measure in cases of hemorrhage, but the best results are obtained if it can be done electively. Indications, however, must be evaluated very carefully in each individual case, especially for thrombosis not associated with cirrhosis of the liver, in which the tendency to a more favorable natural evolution may invite a more conservative approach. The choice of surgical procedures is dictated essentially by the site of obstruction in the portal system. After discussing the indications for various methods, the authors present some cases of thrombosis involving only the superior mesenteric vein, managed successfully by disobliteration and mesenterocaval anastomosis.

Adolescent↗
PubMed1994

Fitness to drive in patients with cirrhosis and portal-systemic shunting: a pilot study evaluating driving performance.

It has been suggested that some patients with cirrhosis are unfit to operate a motor vehicle. However, performance while driving a motor vehicle has not been evaluated in such patients. In this pilot study, we assessed the fitness to drive of stable individuals with cirrhosis and clinical evidence of portal hypertension, portal-systemic shunting and no prior history of hepatic encephalopathy. We examined 15 ambulatory patients with cirrhosis together with 15 age-, educational level- and driving experience-matched healthy controls. Neuropsychological testing was performed with the Reitan trail test, block design and digit symbol tests as well as visual reaction time. A driving test in the laboratory used a film to measure complex visual reaction time (reaction to road symbols) and threat recognition (accident avoidance). Driving on the road was assessed by a licensed Illinois state driving evaluator. Penalty points were given according to 11 standardized driving categories. As a group, patients with cirrhosis had no significant differences in their performance on a simulator or during actual driving conditions when compared to matched controls. Sixty-six percent of the subjects with cirrhosis had two or more abnormal neuropsychological tests, a criterion used to define the presence of subclinical encephalopathy. No deficiencies in simulated or real driving performance was seen when compared to patients with cirrhosis with normal neuropsychological tests. In this study, stable subjects with cirrhosis and evidence of portal hypertension, portal-systemic shunting, abnormal neuropsychological tests and no prior history of overt encephalopathy did not exhibit a major impairment in their fitness to drive.

Adult↗
PubMed1998

[Comparative study of portal-systemic shunt rate measured by formula and radioactive method].

OBJECTIVE: To establish a new simple and useful formula for the observation of portosystemic shunt. METHOD: In the same animals and the same patients, portosystemic shunt rate was measured individually by the two different methods, i.e. formula and radio active method. Using the results of the radio active method as a gold standard, the reliability of the formula method was assessed tested. RESULT: In 11 normal dogs, the portal-systemic shunt rate measured by the formula and radio active methods was 7.03% and 7.55% respectively (P > 0.05). In 9 portosystemic shunting model dogs, the portosystemic shunt rate calculated from the two methods was 48.64% and 51.11% respectively (P > 0.05). In 22 patients with portal hypertension, the preoperative results from the formula and radioactive methods were 52.38% and 55.86% respectively (P > 0.05). In these patients, the postoperative portal-systemic shunt rate was 26.22% and 31.00% respectively (P > 0.05). CONCLUSION: These results fully testified the reliability of the formula method we had established.

Adult↗
PubMed1990

[Measurement of portal systemic circulation by oral and per-rectal administration of I-123 iodoamphetamine].

In an earlier study, we measured the portal circulation noninvasively by Tc-99m pertechnetate per-rectal portal scintigraphy. This method makes it possible to see the portal circulation and to diagnose portal hypertension from the images of the liver and heart. However, the method mainly reflects circulation from the inferior mesenteric vein, the contribution of which to the portal circulation is less than that of the superior mesenteric vein. Here, we devised capsules of I-123 iodoamphetamine (IMP) that dissolve when the pH changes to evaluate the portal circulation arising from the superior mesenteric vein. I-123 IMP enclosed in an enteric-coated capsule was prepared and given orally, just before I-123 IMP was injected into the rectum. The per-rectal portal shunt index (RSI) and oral portal shunt index (OSI) were calculated from the count of radioactivity of the liver and lungs. The RSI and OSI of patients with cirrhosis were both higher than those of the patients with chronic hepatitis. In individual patients, the RSI was higher than the OSI. This noninvasive method seemed to be useful in evaluation of the portal systemic circulation in chronic liver diseases.

Administration, Oral↗
PubMedDate not supplied

Comparison of dietary protein with an oral, branched chain-enriched amino acid supplement in chronic portal-systemic encephalopathy: a randomized controlled trial.

A randomized study was conducted in 37 hospitalized patients at six cooperating hospitals in which protein-intolerant cirrhotic patients were fed increasing amounts of either dietary protein or a branched-chain enriched amino acid solution (BCAA) until they attained an intake of 80 gm protein per day or equivalent or until they developed stage 2 encephalopathy. All patients initially received 20 gm of dietary protein for 1 week, after which 20 gm of protein or BCAA were added weekly. Nitrogen balance improved from negative to positive in all patients in whom it was measured and increased equally in both groups. Seven of the 20 patients in the protein group and 1 of 17 in the BCAA group developed encephalopathy of stage 2 or greater (p less than 0.05). Changes in each component of the portal-systemic encephalopathy syndrome were compared, and differences were statistically significant for mental status grade (p less than 0.01), asterixis (p less than 0.05), Portal-systemic encephalopathy index (p less than 0.01), but insignificant for Number Connection Test, EEG or ammonia. Plasma amino acid profiles showed an increase in BCAA in the study group. Thus, oral BCAA supplements appear to induce positive nitrogen balance to approximately the same degree as an equivalent amount of dietary protein without inducing encephalopathy as frequently.

Adult↗